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10.1016/j.molimm.2020.04.014 http://scihub22266oqcxt.onion/10.1016/j.molimm.2020.04.014 32474254!7519576!32474254     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32474254&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Mol+Immunol 2020 ; 123 (?): 97-105 Nephropedia Template TP {{tp|p=32474254|t=2020. HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis |pdf=|usr=}}{{32474254}} gab.com Text HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis JO: Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32474254 #FOAvip Myeloid-derived suppressor cells (MDSCs) contribute to high mortality rates during sepsis, but how sepsis induces MDSCs is unclear. Previously we reported that microRNA (miR)-21 and miR-181b reprogram MDSCs in septic mice by increasing levels of DNA binding transcription factor, nuclear factor 1 (NFI-A). Here, we provide evidence that miR-21 and miR-181b stabilize NFI-A mRNA and increase NFI-A protein levels by recruiting RNA-binding proteins HuR and Ago1 to its 3' untranslated region (3'UTR). We also find that the NFI-A GU-rich element (GRE)-binding protein CUGBP1 counters miR-21 and miR-181b dependent NFI-A mRNA stabilization and decreases protein production by replacing 3'UTR bound Ago1 with Ago2. We confirmed the miR-21 and miR-181b dependent reprogramming pathway in MDSCs transfected with a luciferase reporter construct containing an NFI-A 3'UTR fragment with point mutations in the miRNA binding sites. These results suggest that targeting NFI-A in MDSCs during sepsis may enhance resistance to uncontrolled infection. Twit Text FOAVip HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis ????Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32474254 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32474254 #FOAvip English Wikipedia <ref>{{Cite pmid|32474254}}</ref> HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis #MMPMID32474254 Bah I; Alkhateeb T; Kumbhare A; Youssef D; Yao ZQ; Hawkin GA; McCall CE; El Gazzar M Mol Immunol 2020[Jul]; 123 (?): 97-105 PMID32474254show ga Myeloid-derived suppressor cells (MDSCs) contribute to high mortality rates during sepsis, but how sepsis induces MDSCs is unclear. Previously we reported that microRNA (miR)-21 and miR-181b reprogram MDSCs in septic mice by increasing levels of DNA binding transcription factor, nuclear factor 1 (NFI-A). Here, we provide evidence that miR-21 and miR-181b stabilize NFI-A mRNA and increase NFI-A protein levels by recruiting RNA-binding proteins HuR and Ago1 to its 3' untranslated region (3'UTR). We also find that the NFI-A GU-rich element (GRE)-binding protein CUGBP1 counters miR-21 and miR-181b dependent NFI-A mRNA stabilization and decreases protein production by replacing 3'UTR bound Ago1 with Ago2. We confirmed the miR-21 and miR-181b dependent reprogramming pathway in MDSCs transfected with a luciferase reporter construct containing an NFI-A 3'UTR fragment with point mutations in the miRNA binding sites. These results suggest that targeting NFI-A in MDSCs during sepsis may enhance resistance to uncontrolled infection. |Animals[MESH] |Cells, Cultured[MESH] |ELAV-Like Protein 1/*physiology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |MicroRNAs/genetics/*physiology[MESH] |Myeloid-Derived Suppressor Cells/*metabolism/pathology[MESH] |NFI Transcription Factors/*genetics/metabolism[MESH] |Sepsis/*genetics/metabolism/pathology[MESH] |Transcriptional Activation[MESH]HuR promotes miRNA-mediated upregulation of NFI-A protein expression i(epmc).pdf DeepDyve Pubget Overpricing